Bilateral paramedian thalamic artery infarcts: report of eight cases.

Abstract

SUMMARY Eight consecutive patients with CT scan evidence of a bilateral infarct in the territory of the paramedian thalamic artery are reported. In seven cases the infarct also extended to the territory of the polar artery. The main symptoms were: (1) disorder of vigilance which cleared in a few days, and hypersomnolence which lasted longer and in two patients was still present a year later; (2) amnesia, detectable clinically in four patients and only with tests in two patients, which persisted in one patient for three years; (3) changes of mood and bulimia present in five and four patients respectively; and (4) vertical gaze paresis in five patients. Only one patient died, and in the remainder the symptoms tended to subside, but none of the patients who could be followed-up for a year returned to normal behaviour. Clinical and CT scan correlations pointed to the mammillo-thalamic tract as the structure whose damage was responsible for the memory disorders.Before computed tomography (CT) infarct of the thalamus was a diagnosis that the clinician could at most suspect, when confronted with a clinical picture resembling the classical Dejerine-Roussy's syndrome,1 but not substantiate in the absence of verification by necropsy. Even more difficult and tentative was the recognition of the other topographical thalamic syndromes that had been reported.2 CT scan has greatly improved our ability to identify in vivo discrete syndromes corresponding to the involvement of the territories supplied by the thalamic arteries. Based on the anatomical description provided by Percheron3 -5 the following types have been identified:6 (1) antero-lateral infarct, associated with polar artery occlusion; (2) postero-lateral infarct, associated with geniculo-thalamic artery occlusion; (3) infero-median infarct, associated with paramedian artery occlusion; and (4) infarct involving the globus pallidus, the posterior limb of the internal capsule and the lateral thalamic nuclei, associated with anterior choroidal artery occlusion.

Total Recovery after Bilateral Paramedian Thalamic Infarct

“…Patients are apathetic, presenting poor insight and slowness of thought [3, 4]. Perseverations and confabulations have been reported [3, 6, 14, 15].…”

“…The onset is acute, with deep stupor or coma, evolving into a lethargic state with hypersomnia. Follow-up of these patients is characterised by a persistent apathy, motor and verbal aspontaneity, anterograde and retrograde amnesia [2, 3, 8]. Vertical voluntary saccades, smooth pursuit and vestibulo-ocular movements are often impaired.…”

“…When the paramedian thalamopeduncular arteries arise from a common trunk [1], arterial occlusion may result in the rare bilateral paramedian thalamomesencephalic infarcts (BPTI), which give rise to vigilance disorders, cognitive deficit and vertical gaze palsy [2, 3, 4, 5, 6, 7, 8]. The onset is acute, with deep stupor or coma, evolving into a lethargic state with hypersomnia.…”

Thalamic Infarcts in Young Adults: Relationship between Clinical-Topographic Features and Pathogenesis

“…In young stroke patients presenting with impairment of consciousness in association with vertical gaze disturbances (the prominent abnormalities in paramedian infarcts) [1, 2, 5, 6, 8, 9, 11, 27, 28], a potential cardiac source of emboli should be suspected first. By contrast, patterns of presentation characterized by sensory deficits, with or without motor impairment, or by prominent neuropsychological disturbances (the hallmarks of infarcts in the territory of the TG pedicle [1, 5, 6, 8, 11, 24, 29, 30]and TTh artery [1, 5, 6, 7, 8, 11, 31], respectively) are more likely to be due to mechanisms other than cardioembolism.…”

Severe Personality Changes after Unilateral Left Paramedian Thalamic Infarct

“…After recovery of consciousness, changes in personality, emotion or behavior are common when paramedian infarcts mainly involve the dorsomedial nucleus (DM) and are usually accompanied by apathy/abulia [2, 4, 5, 6]. Only rarely does a disinhibition syndrome with ‘frontal-like’ disturbances, utilization behavior, bulimia or manic-like delirium develop [3, 4, 5, 6, 7, 8, 9].…”